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Why Turmeric root extract Curcumin may provide health benefits?

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What is the history of Curcumin and Turmeric?

Daily Sabah Health, December 2017
What makes turmeric, which is quite rich in iron and manganese, a key ingredient in alternative medicine is its active ingredient curcumin. Curcumin is one of the best herbs for good health due to large amounts of vitamins C and E. Turmeric is a lightened version of curcumin that can be used in kitchens. Thanks to the curcumin in it, turmeric regulates sleep patterns. It also prevents muscles from getting tired very quickly and boosts sports performance. Some studies indicate that by using turmeric, symptoms can be decreased and inflammation-related conditions, including arthritis, can be eased. Moreover, scientists have proven that consuming turmeric helps to slow down the symptoms of Alzheimer's disease. However, the signature benefit of turmeric is in the treatment of inflammation.

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The oxygen consumption rate (OCR) and extracellularacidification rate (ECAR) of the examined cells were determined bya Seahorse Extracellular Flux XF-24 analyzer (Seahorse Bioscience,North Billerica, MA, USA) according to the manufacturer'sinstructions. Cells (3×10) were seeded in a 24-wellcustom-made plate for the XF-24 analyzer. The culture medium wasreplaced with sodium carbonate-free DMEM (pH 7.4). Prior to theassay, the cell plate and sensor cartridge were kept with 1 mlSeahorse Bioscience XF-24 Calibrant/well in an incubatormaintaining 37°C without CO overnight. The basal,proton-leaked, maximal and non-OXPHOS OCRs were sequentiallymeasured before and after the injection of 75 l ofoligomycin (2 g/ml), FCCP (2 M) or antimycin A (2M), respectively. The program of the Seahorse XF-24analyzer was set according to the manufacturer's instructions. Themitochondrial OCR was calculated by subtracting the residual rateafter injection of antimycin A. The OCR and ECAR were expressed inpmol/min and mpH/min, respectively, and normalized to the examinedcell number.

1155 Sixteenth Street N.W.Washington, DC 20036

1155 Sixteenth Street N.W.Washington, DC 20036

Protein synthesis inhibitors Many therapeutically useful antibiotics owe their action to inhibition of some step in the complex process of translation. Their attack is always at one of the events occurring on the ribosome and rather than the stage of amino acid activation or attachment to a particular tRNA. Most have an affinity or specificity for 70S (as opposed to 80S) ribosomes, and they achieve their selective toxicity in this manner. The most important antibiotics with this mode of action are the tetracyclines, chloramphenicol, the macrolides (e.g. erythromycin) and the aminoglycosides (e.g. streptomycin).

Cell membrane inhibitors disorganize the structure or inhibit the function of bacterial membranes. The integrity of the cytoplasmic and outer membranes is vital to bacteria, and compounds that disorganize the membranes rapidly kill the cells. However, due to the similarities in phospholipids in eubacterial and eukaryotic membranes, this action is rarely specific enough to permit these compounds to be used systemically. The only antibacterial antibiotic of clinical importance that acts by this mechanism is Polymyxin, produced by Bacillus polymyxis. Polymyxin is effective mainly against Gram-negative bacteria and is usually limited to topical usage. Polymyxins bind to membrane phospholipids and thereby interfere with membrane function. Polymyxin is occasionally given for urinary tract infections caused by Pseudomonas that are gentamicin, carbenicillin and tobramycin resistant. The balance between effectiveness and damage to the kidney and other organs is dangerously close, and the drug should only be given under close supervision in the hospital.


Chavan Dilip V.*, Mulaje S. S.1, Mohalkar R.Y.1

Journal of Cellular Biochemistry, August 2017
The effect of curcumin on inhibiting cancer has been recognized, but the mechanism remains elusive. This study tests a hypothesis that administration of curcumin down regulates Tregs in lung cancer (LC) patients. In this study, a group of LC patients was treated with curcumin. The peripheral Tregs and T helper (Th) 1 cells were analyzed by flow cytometry. The mechanism by which curcumin regulated the Tregs was observed by cell culture approaches. The results showed that the frequency of peripheral Treg was markedly higher in LC patients than that in healthy subjects, which was suppressed after treating with curcumin for 2 weeks. The peripheral Th1 cells were increased in LC patients after the curcumin therapy. The data of the in vitro experiments showed that curcumin converted the LC patient-isolated Tregs to Th1 cells via repressing the gene transcription of forkhead protein-3 and increasing the expression of interferon-γ. In conclusion, curcumin can convert LC patient-isolated Tregs to Th1 cells. The results suggest that curcumin may improve the antitumor immunity by regulating the tumor specific immune tolerance.

In conclusion, we found that HCC cells which exhibithigher glycolysis and lower mitochondrial respiration are moreresistant to mitochondrial inhibitors and biguanide drugs. Ourfindings also provide evidence to suggest that altering the energymetabolism from aerobic glycolysis to OXPHOS enhances the cellsensitivity to biguanides. These findings suggest that a change inenergy metabolism from glycolysis to OXPHOS enhances the effect ofbiguanide drugs in HCC therapy.

Actinomycetes, Enzymes, Antibiotics, GC content etc
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  • Occurrence & habitats of Actinomycetes:

    Antibiotics are molecules that ..

  • DANS is an institute of KNAW and NWO

    Inhibition of Cell Wall Biosynthesis

  • Enzymes present in Actinomycetes:

    Antibiotics that inhibit cell wall biosynthesis induce ..

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Applications of different enzymes:

Replacing glucose with galactoseincreases the response to mitochondrial inhibitors and biguanidesin regards to AMPK-mTOR signaling in HCC cells. HCC cell lines(HepG2, Mahlavu, SK-HEP-1 and HA22T/VGH) were cultured in DMEM with25 mM glucose or galactose, and then treated with (A and B)mitochondrial inhibitors (0.2 μM rotenone (R) and 1μg/ml oligomycin (O)] for 3 h or (C and D) biguanide drugs(5 mM metformin for 9 h, and 0.1 mM phenformin for 0, 2, 4 and 6h), and the AMPK and mTOR signaling was analyzed using westernblotting with antibodies specific for p-p70S6K,p70S6K, p-4E-BP-1, 4E-BP-1, p-AMPK, AMPK, p-Raptor andRaptor. α-tubulin was used as an internal control for proteinloading. Each western blot shown is a representative resultobtained from three independent experiments. AMPK, AMP-activatedprotein kinase; HCC, hepatocellular carcinoma.

Applications of Microbial lipases 19, 29:

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Chavan Dilip V.*, Mulaje S. S., Mohalkar R.Y.

Medical News Today, August 2017
A common obstacle in the treatment of pancreatic cancer is drug resistance. However, new research has shown that curcumin - a compound that can be found in turmeric - can help to overcome the resistance to chemotherapy. Curcumin is the active compound found in plants such as turmeric, and more and more studies have been pointing to the therapeutic potential of the compound for various conditions, ranging from cancer to diabetes. Preclinical studies have suggested that the compound has various antioxidant, neuroprotective, anti-inflammatory, and anticarcinogenic properties. "By treating certain cells with small doses of curcumin, we were able to reverse the pathways that lead to chemoresistance," says Dr. Goel. "This is an important breakthrough that could lead to better prognosis and longer lives for patients with chemoresistant pancreatic cancer." Previous studies have shown that curcumin has preventative benefits, but to the authors' knowledge, this is the first study that shows the beneficial effect of the plant extract in combination with chemotherapy and its advantages in overcoming drug resistance.


Replacing glucose with galactosesensitizes the HCC cell lines to mitochondrial inhibitors andbiguanides. HCC cell lines (HepG2, Mahlavu, SK-HEP-1 and HA22T/VGH)were cultured in DMEM medium with 25 mM glucose or galactose, andthen treated with (A and B) mitochondrial inhibitors (rotenone andoligomycin) or (C and D) biguanide drugs (metformin and phenformin)at different doses for 24 h, and the cytotoxicity was analyzedusing the SRB assay. HCC, hepatocellular carcinoma; SRB,sulforhodamine B.

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